Abstract
We investigated the expression of transforming growth factors β1 and α (TGF-β1, TGF-α in hormone-responsive (MPA-R) and unresponsive (MPA-U) tumor lines obtained from medroxyprogesterone acetate (MPA)-induced mammary adenocarcinomas in BALBIc mice. The tumors were transplanted into MPA-treated and untreated mice. TGF-β1 gene expression was observed in the MPA-R lines growing in untreated animals, but not in MPA-treated mice. TGF-β1 mRNA was not detected in the MPA-U tumor lines growing in either MPA-treated or untreated animals. In MPA-R lines the levels of TGF-β1 expression were inversely correlated to growth rate. High-affinity TGF-β1 receptors were present in the MPA-R tumors. These results suggest that one of the mechanisms by which MP A exerts its proliferative effect on MPA-R tumor lines is inhibition of the expression of TGF-β1. Thus, the lack of expression of TGF-β1 in MPA-U tumors may be related to the acquisition of autonomous growth.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 173-180 |
| Number of pages | 8 |
| Journal | Cancer Investigation |
| Volume | 13 |
| Issue number | 2 |
| DOIs | |
| State | Published - 1995 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Cancer Research
- Oncology
Cite this
Correlation of TGF-(si expression with medroxiprogesterone acetate responsiveness in mouse mammary adenocarcinomas. / Elizalde, Patricia V.; Guerra, Fabiana K.; Gravano, Martin; Lanari, Claudia; Lippman, Marc E.; Charreau, Eduardo H.; Lupu, Ruth.
In: Cancer Investigation, Vol. 13, No. 2, 1995, p. 173-180.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Correlation of TGF-(si expression with medroxiprogesterone acetate responsiveness in mouse mammary adenocarcinomas
AU - Elizalde, Patricia V.
AU - Guerra, Fabiana K.
AU - Gravano, Martin
AU - Lanari, Claudia
AU - Lippman, Marc E.
AU - Charreau, Eduardo H.
AU - Lupu, Ruth
PY - 1995
Y1 - 1995
N2 - We investigated the expression of transforming growth factors β1 and α (TGF-β1, TGF-α in hormone-responsive (MPA-R) and unresponsive (MPA-U) tumor lines obtained from medroxyprogesterone acetate (MPA)-induced mammary adenocarcinomas in BALBIc mice. The tumors were transplanted into MPA-treated and untreated mice. TGF-β1 gene expression was observed in the MPA-R lines growing in untreated animals, but not in MPA-treated mice. TGF-β1 mRNA was not detected in the MPA-U tumor lines growing in either MPA-treated or untreated animals. In MPA-R lines the levels of TGF-β1 expression were inversely correlated to growth rate. High-affinity TGF-β1 receptors were present in the MPA-R tumors. These results suggest that one of the mechanisms by which MP A exerts its proliferative effect on MPA-R tumor lines is inhibition of the expression of TGF-β1. Thus, the lack of expression of TGF-β1 in MPA-U tumors may be related to the acquisition of autonomous growth.
AB - We investigated the expression of transforming growth factors β1 and α (TGF-β1, TGF-α in hormone-responsive (MPA-R) and unresponsive (MPA-U) tumor lines obtained from medroxyprogesterone acetate (MPA)-induced mammary adenocarcinomas in BALBIc mice. The tumors were transplanted into MPA-treated and untreated mice. TGF-β1 gene expression was observed in the MPA-R lines growing in untreated animals, but not in MPA-treated mice. TGF-β1 mRNA was not detected in the MPA-U tumor lines growing in either MPA-treated or untreated animals. In MPA-R lines the levels of TGF-β1 expression were inversely correlated to growth rate. High-affinity TGF-β1 receptors were present in the MPA-R tumors. These results suggest that one of the mechanisms by which MP A exerts its proliferative effect on MPA-R tumor lines is inhibition of the expression of TGF-β1. Thus, the lack of expression of TGF-β1 in MPA-U tumors may be related to the acquisition of autonomous growth.
UR - http://www.scopus.com/inward/record.url?scp=0028927483&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0028927483&partnerID=8YFLogxK
U2 - 10.3109/07357909509011687
DO - 10.3109/07357909509011687
M3 - Article
C2 - 7874571
AN - SCOPUS:0028927483
VL - 13
SP - 173
EP - 180
JO - Cancer Investigation
JF - Cancer Investigation
SN - 0735-7907
IS - 2
ER -